Literature DB >> 3414491

Increased left ventricular diastolic stiffness in the early phase of hereditary cardiomyopathy.

V I Kapelko1, W W Parmley, S Wu, R D Stone, G Jasmin, J Wikman-Coffelt.   

Abstract

Isolated hearts from normal and cardiomyopathic hamsters (160 to 180 days of age) were perfused through the aorta and assessed by echocardiographic and 31P-NMR (nuclear magnetic resonance) techniques. A decreased left ventricular systolic pressure in cardiomyopathic hamsters was associated with diminished cardiac size and left ventricular wall thickness. However, the ratio of inner/outer cross-sectional area and estimated left ventricular volume at any given left ventricular weight was significantly higher, indicating relative left ventricular chamber enlargement in cardiomyopathic hamsters. Left ventricular volumes were increased with an intraventricular balloon. Gradual inflation of the balloon resulted in increments of left ventricular systolic and developed stress that rose to the same values in both groups. At this point, the normalized stress-strain relationship was approximately two times steeper for cardiomyopathic hamsters, while at lower strain values the diastolic stress in cardiomyopathic hamsters was less than in controls, possibly due to cardiac dilatation. Almost the same degree of dilatation was induced in control hearts by the acute addition of 1% alcohol, but it was not followed by increased diastolic stiffness. Examination of hearts by 31P-NMR techniques revealed a decreased phosphocreatine/inorganic phosphate (PCr/Pi) ratio in the cardiomyopathic hamsters that progressed further with balloon inflation and was associated with a relative fall in PCr and adenosine triphosphate (ATP) content. Results suggest increased diastolic stiffness in cardiomyopathic hamsters, which was not seen in acute cardiac depression with alcohol. Diastolic volume overload with increased wall stress is probably the major factor contributing to increased diastolic stiffness early in the cardiomyopathy.

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Year:  1988        PMID: 3414491     DOI: 10.1016/0002-8703(88)90335-3

Source DB:  PubMed          Journal:  Am Heart J        ISSN: 0002-8703            Impact factor:   4.749


  5 in total

Review 1.  Myofibrillar creatine kinase and cardiac contraction.

Authors:  R Ventura-Clapier; V Veksler; J A Hoerter
Journal:  Mol Cell Biochem       Date:  1994 Apr-May       Impact factor: 3.396

2.  Glycolysis in heart failure: a 31P-NMR and surface fluorometry study.

Authors:  W Auffermann; S T Wu; W W Parmley; J Wikman-Coffelt
Journal:  Basic Res Cardiol       Date:  1990 Jul-Aug       Impact factor: 17.165

Review 3.  In situ study of myofibrils, mitochondria and bound creatine kinases in experimental cardiomyopathies.

Authors:  V Veksler; R Ventura-Clapier
Journal:  Mol Cell Biochem       Date:  1994 Apr-May       Impact factor: 3.396

4.  Cellular hypertrophy in cardiomyopathic patients is associated with lower creatine-stimulated mitochondrial respiration.

Authors:  M Popovich; S Kostin; T Branishte; V Kobets; V Kapelko
Journal:  Mol Cell Biochem       Date:  1995-02-09       Impact factor: 3.396

5.  Distinct modulation of myocardial performance, energy metabolism, and [Ca2+]i transients by positive inotropic drugs in normal and severely failing hamster hearts.

Authors:  P T Buser; S Y Wu; W W Parmley; G Jasmin; J Wikman-Coffelt
Journal:  Cardiovasc Drugs Ther       Date:  1995-02       Impact factor: 3.727

  5 in total

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